摘要
目的 研究γIP 1 0和Mig通过趋化因子CXC受体 3 (CXCR3 )激活嗜酸性粒细胞的活化细胞核因子 (nuclearfactorofactivatedTlymphocytes,NFAT)作用。方法 嗜酸性粒细胞的纯化技术、流式细胞术、实时定量逆转录PCR (RT PCR)、核提取物和电泳移动性转变测定等方法进行测定与分析。结果 CXCR3大量在嗜酸性粒细胞上表达。通过流式细胞仪及实时定量RT PCR技术检测证明 ,IL 2和IL 1 0上调或下调嗜酸性粒细胞上CXCR3的蛋白和mRNA表达水平。其配体γIP 1 0和Mig可以引起嗜酸性粒细胞中的NFAT复合体的核易位而激活NFAT1和NFAT4。结论 CXCR3 γIP 1 0和 Mig受体 配体以及IL 2和IL 1 0对CXCR3表达的调节作用可能在过敏炎症过程 (包括启动、发展和结局的病理生理过程 )的细胞因子 /趋化因子环境中发挥特别重要的作用。
Objective To investigate γ IP 10 and Mig activate NFAT(nuclear factor of activated T lymphocytes) through CXCR3 on eosinophils. Methods Negative eosinophil purification, flow cytometry, real time quantitative reverse transcription (RT) PCR assay, and electrophretic mobility shift assay. Results CXCR3 was found to be expressed on eosinophils. CXCR3 protein and mRNA expression in eosinophils were up and down regulated by IL 2 and IL 10. γ IP 10 and Mig stimulate activation of NFAT1 and NFAT4 in eosinophils in terms of NFAT complex nuclear translocation. Conclusion CXCR3 γ IP 10 and Mig receptor ligand pairs as well as the effects of IL 2 and IL 10 on them may be especially important as cytokine/chemokine environment for the pathogenesis of allergic inflammation including its initiation, progression and termination in the processes.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2001年第5期510-515,共6页
Chinese Journal of Microbiology and Immunology
基金
国家自然科学基金 ( 39870 674)
安徽省自然科学基金( 98436630 )
安徽省教育厅科学研究基金 ( 98JL0 63)资助项目
